Relationships between nitric oxide biomarkers and physiological outcomes following dietary nitrate supplementation.

Dietary nitrate (NO3-) supplementation can increase nitric oxide (NO) bioavailability, reduce blood pressure (BP) and improve muscle contractile function in humans. Plasma nitrite concentration (plasma [NO2-]) is the most oft-used biomarker of NO bioavailability. However, it is unclear which of several NO biomarkers (NO3-, NO2-, S-nitrosothiols (RSNOs)) in plasma, whole blood (WB), red blood cells (RBC) and skeletal muscle correlate with the physiological effects of acute and chronic dietary NO3- supplementation. Using a randomized, double-blind, crossover design, 12 participants (9 males) consumed NO3--rich beetroot juice (BR) (∼12.8 mmol NO3-) and NO3--depleted placebo beetroot juice (PL) acutely and then chronically (for two weeks). Biological samples were collected, resting BP was assessed, and 10 maximal voluntary isometric contractions of the knee extensors were performed at 2.5-3.5 h following supplement ingestion on day 1 and day 14. Diastolic BP was significantly lower in BR (-2 ± 3 mmHg, P = 0.03) compared to PL following acute supplementation, while the absolute rate of torque development (RTD) was significantly greater in BR at 0-30 ms (39 ± 57 N m s-1, P = 0.03) and 0-50 ms (79 ± 99 N m s-1, P = 0.02) compared to PL following two weeks supplementation. Greater WB [RSNOs] rather than plasma [NO2-] was correlated with lower diastolic BP (r = -0.68, P = 0.02) in BR compared to PL following acute supplementation, while greater skeletal muscle [NO3-] was correlated with greater RTD at 0-30 ms (r = 0.64, P=0.03) in BR compared to PL following chronic supplementation. We conclude that [RSNOs] in blood, and [NO3-] in skeletal muscle, are relevant biomarkers of NO bioavailability which are related to the reduction of BP and the enhanced muscle contractile function following dietary NO3- ingestion in humans.

Reduction in blood pressure following acute dietary nitrate ingestion is correlated with increased red blood cell S-nitrosothiol concentrations.

Dietary nitrate (NO3-) supplementation can enhance nitric oxide (NO) bioavailability and lower blood pressure (BP) in humans. The nitrite concentration ([NO2-]) in the plasma is the most commonly used biomarker of increased NO availability. However, it is unknown to what extent changes in other NO congeners, such as S-nitrosothiols (RSNOs), and in other blood components, such as red blood cells (RBC), also contribute to the BP lowering effects of dietary NO3-. We investigated the correlations between changes in NO biomarkers in different blood compartments and changes in BP variables following acute NO3- ingestion. Resting BP was measured and blood samples were collected at baseline, and at 1, 2, 3, 4 and 24 h following acute beetroot juice (∼12.8 mmol NO3-, ∼11 mg NO3-/kg) ingestion in 20 healthy volunteers. Spearman rank correlation coefficients were determined between the peak individual increases in NO biomarkers (NO3-, NO2-, RSNOs) in plasma, RBC and whole blood, and corresponding decreases in resting BP variables. No significant correlation was observed between increased plasma [NO2-] and reduced BP, but increased RBC [NO2-] was correlated with decreased systolic BP (rs = -0.50, P = 0.03). Notably, increased RBC [RSNOs] was significantly correlated with decreases in systolic (rs = -0.68, P = 0.001), diastolic (rs = -0.59, P = 0.008) and mean arterial pressure (rs = -0.64, P = 0.003). Fisher's z transformation indicated no difference in the strength of the correlations between increases in RBC [NO2-] or [RSNOs] and decreased systolic blood pressure. In conclusion, increased RBC [RSNOs] may be an important mediator of the reduction in resting BP observed following dietary NO3- supplementation.

Time course of human skeletal muscle nitrate and nitrite concentration changes following dietary nitrate ingestion.

Dietary nitrate (NO3-) ingestion can be beneficial for health and exercise performance. Recently, based on animal and limited human studies, a skeletal muscle NO3- reservoir has been suggested to be important in whole body nitric oxide (NO) homeostasis. The purpose of this study was to determine the time course of changes in human skeletal muscle NO3- concentration ([NO3-]) following the ingestion of dietary NO3-. Sixteen participants were allocated to either an experimental group (NIT: n = 11) which consumed a bolus of ∼1300 mg (12.8 mmol) potassium nitrate (KNO3), or a placebo group (PLA: n = 5) which consumed a bolus of potassium chloride (KCl). Biological samples (muscle (vastus lateralis), blood, saliva and urine) were collected shortly before NIT or PLA ingestion and at intervals over the course of the subsequent 24 h. At baseline, no differences were observed for muscle [NO3-] and [NO2-] between NIT and PLA (P > 0.05). In PLA, there were no changes in muscle [NO3-] or [NO2-] over time. In NIT, muscle [NO3-] was significantly elevated above baseline (54 ± 29 nmol/g) at 0.5 h, reached a peak at 3 h (181 ± 128 nmol/g), and was not different to baseline from 9 h onwards (P > 0.05). Muscle [NO2-] did not change significantly over time. Following ingestion of a bolus of dietary NO3-, skeletal muscle [NO3-] increases rapidly, reaches a peak at ∼3 h and subsequently declines towards baseline values. Following dietary NO3- ingestion, human m. vastus lateralis [NO3-] expressed a slightly delayed pharmacokinetic profile compared to plasma [NO3-].

Skeletal Muscle Nitrate as a Regulator of Systemic Nitric Oxide Homeostasis.

Nonenzymatic nitric oxide (NO) generation via the reduction of nitrate and nitrite ions, along with remarkably high levels of nitrate ions in skeletal muscle, have been described recently. Skeletal muscle nitrate storage may be critical for maintenance of NO homeostasis in healthy aging, and nitrate supplementation may be useful for the treatment of specific pathophysiologies and for enhancing normal functions.

Effects of dietary nitrate on the O2 cost of submaximal exercise: Accounting for "noise" in pulmonary gas exchange measurements.

Dietary nitrate (NO3-) supplementation can reduce the oxygen cost of submaximal exercise, but this has not been reported consistently. We hypothesised that the number of step transitions to moderate-intensity exercise, and corresponding effects on the signal-to-noise ratio for pulmonary V˙ O2, may be important in this regard. Twelve recreationally active participants were assigned in a randomised, double-blind, crossover design to supplement for 4 days in three conditions: 1) control (CON; water); 2); PL (NO3--depleted beetroot juice); and 3) BR (NO3--rich beetroot juice). On days 3 and 4, participants completed two 6-min step transitions to moderate-intensity cycle exercise. Breath-by-breath V˙ O2 data were collected and V˙ O2 kinetic responses were determined for a single transition and when the responses to 2, 3 and 4 transitions were ensemble-averaged. Steady-state V˙ O2 was not different between PL and BR when the V˙ O2 response to one-, two- or three-step transition was compared but was significantly lower in BR compared to PL when four-step transitions was considered (PL: 1.33 ± 0.34 vs. BR: 1.31 ± 0.34 L·min-1, P < 0.05). There were no differences in pulmonary V˙ O2 responses between CON and PL (P > 0.05). Multiple step transitions may be required to detect the influence of NO3- supplementation on steady-state V˙ O2.

Physiological and performance effects of dietary nitrate and N-acetylcysteine supplementation during prolonged heavy-intensity cycling.

The purpose of this study was to investigate effects of concurrent and independent administration of dietary nitrate (NO3-), administered as NO3--rich beetroot juice (BR; ~12.4 mmol of NO3-), and N-acetylcysteine (NAC; 70 mg·kg-1) on physiological responses during prolonged exercise and subsequent high-intensity exercise tolerance. Sixteen recreationally active males supplemented with NO3--depleted beetroot juice (PL) or BR for 6 days and ingested an acute dose of NAC or maltodextrin (MAL) 1 h prior to performing 1 h of heavy-intensity cycling exercise immediately followed by a severe-intensity time-to-exhaustion (TTE) test in four conditions: 1) PL+MAL, 2) PL+NAC, 3) BR+MAL and 4) BR+NAC. Pre-exercise plasma [NO3-] and nitrite ([NO2-]) were elevated following BR+NAC  and BR+MAL (both P < 0.01) compared with PL+NAC and PL+MAL; plasma [cysteine] was increased in PL+NAC  and BR+NAC (both P < 0.01) compared to PL+MAL. Muscle excitability declined over time during the prolonged cycling bout in all conditions  but was better preserved in PL+NAC  compared to BR+NAC (P < 0.01) and PL+MAL (P < 0.05). There was no effect of supplementation on subsequent TTE . These findings indicate that co-ingestion of BR and NAC does not appreciably alter physiological responses during prolonged heavy-intensity cycling or enhance subsequent exercise tolerance.

Steady-state [Formula: see text] above MLSS: evidence that critical speed better represents maximal metabolic steady state in well-trained runners.

The metabolic boundary separating the heavy-intensity and severe-intensity exercise domains is of scientific and practical interest but there is controversy concerning whether the maximal lactate steady state (MLSS) or critical power (synonymous with critical speed, CS) better represents this boundary. We measured the running speeds at MLSS and CS and investigated their ability to discriminate speeds at which [Formula: see text] was stable over time from speeds at which a steady-state [Formula: see text] could not be established. Ten well-trained male distance runners completed 9-12 constant-speed treadmill tests, including 3-5 runs of up to 30-min duration for the assessment of MLSS and at least 4 runs performed to the limit of tolerance for assessment of CS. The running speeds at CS and MLSS were significantly different (16.4 ± 1.3 vs. 15.2 ± 0.9 km/h, respectively; P < 0.001). Blood lactate concentration was higher and increased with time at a speed 0.5 km/h higher than MLSS compared to MLSS (P < 0.01); however, pulmonary [Formula: see text] did not change significantly between 10 and 30 min at either MLSS or MLSS + 0.5 km/h. In contrast, [Formula: see text] increased significantly over time and reached [Formula: see text] at end-exercise at a speed ~ 0.4 km/h above CS (P < 0.05) but remained stable at a speed ~ 0.5 km/h below CS. The stability of [Formula: see text] at a speed exceeding MLSS suggests that MLSS underestimates the maximal metabolic steady state. These results indicate that CS more closely represents the maximal metabolic steady state when the latter is appropriately defined according to the ability to stabilise pulmonary [Formula: see text].

Stem emissions of monoterpenes, acetaldehyde and methanol from Scots pine (Pinus sylvestris L.) affected by tree-water relations and cambial growth.

Tree stems are an overlooked source of volatile organic compounds (VOCs). Their contribution to ecosystem processes and total VOC fluxes is not well studied, and assessing it requires better understanding of stem emission dynamics and their driving processes. To gain more mechanistic insight into stem emission patterns, we measured monoterpene, methanol and acetaldehyde emissions from the stems of mature Scots pines (Pinus sylvestris L.) in a boreal forest over three summers. We analysed the effects of temperature, soil water content, tree water status, transpiration and growth on the VOC emissions and used generalized linear models to test their relative importance in explaining the emissions. We show that Scots pine stems are considerable sources of monoterpenes, methanol and acetaldehyde, and their emissions are strongly regulated by temperature. However, even small changes in water availability affected the emission potentials: increased soil water content increased the monoterpene emissions within a day, whereas acetaldehyde and methanol emissions responded within 2-4 days. This lag corresponded to their transport time in the xylem sap from the roots to the stem. Moreover, the emissions of monoterpenes, methanol and acetaldehyde were influenced by the cambial growth rate of the stem with 6-10-day lags.

Human skeletal muscle nitrate store: influence of dietary nitrate supplementation and exercise.

KEY POINTS: Nitric oxide (NO), a potent vasodilator and a regulator of many physiological processes, is produced in mammals both enzymatically and by reduction of nitrite and nitrate ions. We have previously reported that, in rodents, skeletal muscle serves as a nitrate reservoir, with nitrate levels greatly exceeding those in blood or other internal organs, and with nitrate being reduced to NO during exercise. In the current study, we show that nitrate concentration is substantially greater in skeletal muscle than in blood and is elevated further by dietary nitrate ingestion in human volunteers. We also show that high-intensity exercise results in a reduction in the skeletal muscle nitrate store following supplementation, likely as a consequence of its reduction to nitrite and NO. We also report the presence of sialin, a nitrate transporter, and xanthine oxidoreductase in human skeletal muscle, indicating that muscle has the necessary apparatus for nitrate transport, storage and metabolism. ABSTRACT: Rodent skeletal muscle contains a large store of nitrate that can be augmented by the consumption of dietary nitrate. This muscle nitrate reservoir has been found to be an important source of nitrite and nitric oxide (NO) via its reduction by tissue xanthine oxidoreductase. To explore if this pathway is also active in human skeletal muscle during exercise, and if it is sensitive to local nitrate availability, we assessed exercise-induced changes in muscle nitrate and nitrite concentrations in young healthy humans, under baseline conditions and following dietary nitrate consumption. We found that baseline nitrate and nitrite concentrations were far higher in muscle than in plasma (∼4-fold and ∼29-fold, respectively), and that the consumption of a single bolus of dietary nitrate (12.8 mmol) significantly elevated nitrate concentration in both plasma (∼19-fold) and muscle (∼5-fold). Consistent with these observations, and with previous suggestions of active muscle nitrate transport, we present western blot data to show significant expression of the active nitrate/nitrite transporter sialin in human skeletal muscle. Furthermore, we report an exercise-induced reduction in human muscle nitrate concentration (by ∼39%), but only in the presence of an increased muscle nitrate store. Our results indicate that human skeletal muscle nitrate stores are sensitive to dietary nitrate intake and may contribute to NO generation during exercise. Together, these findings suggest that skeletal muscle plays an important role in the transport, storage and metabolism of nitrate in humans.

Dietary Nitrate and Physical Performance.

Nitric oxide (NO) plays a plethora of important roles in the human body. Insufficient production of NO (for example, during older age and in various disease conditions) can adversely impact health and physical performance. In addition to its endogenous production through the oxidation of l-arginine, NO can be formed nonenzymatically via the reduction of nitrate and nitrite, and the storage of these anions can be augmented by the consumption of nitrate-rich foodstuffs such as green leafy vegetables. Recent studies indicate that dietary nitrate supplementation, administered most commonly in the form of beetroot juice, can ( a) improve muscle efficiency by reducing the O2 cost of submaximal exercise and thereby improve endurance exercise performance and ( b) enhance skeletal muscle contractile function and thereby improve muscle power and sprint exercise performance. This review describes the physiological mechanisms potentially responsible for these effects, outlines the circumstances in which ergogenic effects are most likely to be evident, and discusses the effects of dietary nitrate supplementation on physical performance in a range of human populations.

Contralateral fatigue during severe-intensity single-leg exercise: influence of acute acetaminophen ingestion.

Exhaustive single-leg exercise has been suggested to reduce time to task failure (Tlim) during subsequent exercise in the contralateral leg by exacerbating central fatigue development. We investigated the influence of acetaminophen (ACT), an analgesic that may blunt central fatigue development, on Tlim during single-leg exercise completed with and without prior fatiguing exercise of the contralateral leg. Fourteen recreationally active men performed single-leg severe-intensity knee-extensor exercise to Tlim on the left (Leg1) and right (Leg2) legs without prior contralateral fatigue and on Leg2 immediately following Leg1 (Leg2-CONTRA). The tests were completed following ingestion of 1-g ACT or maltodextrin [placebo (PL)] capsules. Intramuscular phosphorus-containing metabolites and substrates and muscle activation were assessed using 31P-MRS and electromyography, respectively. Tlim was not different between Leg1ACT and Leg1PL conditions (402 ± 101 vs. 390 ± 106 s, P = 0.11). There was also no difference in Tlim between Leg2ACT-CONTRA and Leg2PL-CONTRA (324 ± 85 vs. 311 ± 92 s, P = 0.10), but Tlim was shorter in Leg2ACT-CONTRA and Leg2PL-CONTRA than in Leg2CON (385 ± 104 s, both P < 0.05). There were no differences in intramuscular phosphorus-containing metabolites and substrates or muscle activation between Leg1ACT and Leg1PL and between Leg2ACT-CONTRA and Leg2PL-CONTRA (all P > 0.05). These findings suggest that levels of metabolic perturbation and muscle activation at Tlim are not different during single-leg severe-intensity knee-extensor exercise completed with or without prior fatiguing exercise of the contralateral leg. Despite contralateral fatigue, ACT ingestion did not alter neuromuscular responses, muscle metabolites, or exercise performance.

Changes in the power-duration relationship following prolonged exercise: estimation using conventional and all-out protocols and relationship with muscle glycogen.

It is not clear how the parameters of the power-duration relationship [critical power (CP) and W'] are influenced by the performance of prolonged endurance exercise. We used severe-intensity prediction trials (conventional protocol) and the 3-min all-out test (3MT) to measure CP and W' following 2 h of heavy-intensity cycling exercise and took muscle biopsies to investigate possible relationships to changes in muscle glycogen concentration ([glycogen]). Fourteen participants completed a rested 3MT to establish end-test power (Control-EP) and work done above EP (Control-WEP). Subsequently, on separate days, immediately following 2 h of heavy-intensity exercise, participants completed a 3MT to establish Fatigued-EP and Fatigued-WEP and three severe-intensity prediction trials to the limit of tolerance (Tlim) to establish Fatigued-CP and Fatigued-W'. A muscle biopsy was collected immediately before and after one of the 2-h exercise bouts. Fatigued-CP (256 ± 41 W) and Fatigued-EP (256 ± 52 W), and Fatigued-W' (15.3 ± 5.0 kJ) and Fatigued-WEP (14.6 ± 5.3 kJ), were not different (P > 0.05) but were ~11% and ~20% lower than Control-EP (287 ± 46 W) and Control-WEP (18.7 ± 4.7 kJ), respectively (P < 0.05). The change in muscle [glycogen] was not significantly correlated with the changes in either EP (r = 0.19) or WEP (r = 0.07). The power-duration relationship is adversely impacted by prolonged endurance exercise. The 3MT provides valid estimates of CP and W' following 2 h of heavy-intensity exercise, but the changes in these parameters are not primarily determined by changes in muscle [glycogen].

Time-trial performance is not impaired in either competitive athletes or untrained individuals following a prolonged cognitive task.

It has been reported that mental fatigue decreases exercise performance during high-intensity constant-work-rate exercise (CWR) and self-paced time trials (TT) in recreationally-trained individuals. The purpose of this study was to determine whether performance is impaired following a prolonged cognitive task in individuals trained for competitive sport. Ten trained competitive athletes (ATH) and ten untrained healthy men (UNT) completed a 6-min severe-intensity CWR followed by a 6-min cycling TT immediately following cognitive tasks designed to either perturb (Stroop colour-word task and N-back task; PCT) or maintain a neutral (documentary watching; CON) mental state. UNT had a higher heart rate (75 ± 9 v. 69 ± 7 bpm; P = 0.002) and a lower positive affect PANAS score (19.9 ± 7.5 v. 24.3 ± 4.6; P = 0.036) for PCT compared to CON. ATH showed no difference in heart rate, but had a higher negative affect score for PCT compared to CON (15.1 ± 3.7 v. 12.2 ± 2.7; P = 0.029). Pulmonary O2 uptake during CWR was not different between PCT and CON for ATH or UNT. Work completed during TT was not different between PCT and CON for ATH (PCT 103 ± 12 kJ; CON 102 ± 12 kJ; P > 0.05) or UNT (PCT 75 ± 11 kJ; CON 74 ± 12 kJ; P > 0.05). Compared to CON, during PCT, UNT showed unchanged psychological stress responses, whereas ATH demonstrated increased psychological stress responses. However, regardless of this distinction, exercise performance was not affected by PCT in either competitive athletes or untrained individuals.

Road cycle TT performance: Relationship to the power-duration model and association with FTP.

PURPOSE: To determine the accuracy of critical power (CP) and W' (the curvature constant of the power-duration relationship) derived from self-paced time-trial (TT) prediction trials using mobile power meters to predict 16.1-km road cycling TT performance. This study also aimed to assess the agreement between functional threshold power (FTP) and CP. METHODS: Twelve competitive male cyclists completed an incremental test to exhaustion, a FTP test and 4-5 self-paced TT bouts on a stationary bike within the lab, and a 16.1 km road TT, using mobile power meters. RESULTS: CP and W' derived from the power-duration relationship closely predicted TT performance. The 16.1-km road TT completion time (26.7 ± 2.2 min) was not significantly different from and was significantly correlated with the predicted time-to-completion (27.5 ± 3.3 min, r = 0.89, P < 0.01). CP and FTP were not significantly different (275 ± 40 W vs. 278 ± 42 W, P > 0.05); however, the limits of agreement between CP and FTP were 30 to -36 W. DISCUSSION: The findings of this study indicate that CP and W' determined using mobile power meters during maximal, self-paced TT prediction trials can be used to accurately predict 16.1-km cycling performance, supporting the application of the CP and W' for performance prediction. However, the limits of agreement were too large to consider FTP and CP interchangeable.

Influence of dietary nitrate food forms on nitrate metabolism and blood pressure in healthy normotensive adults.

Inorganic nitrate (NO3-) supplementation has been shown to improve cardiovascular health indices in healthy adults. The purpose of this study was to investigate how the vehicle of NO3- administration can influence NO3- metabolism and the subsequent blood pressure response. Ten healthy males consumed an acute equimolar dose of NO3- (∼5.76 mmol) in the form of a concentrated beetroot juice drink (BR; 55 mL), a non-concentrated beetroot juice drink (BL; 456 mL) and a solid beetroot flapjack (BF; 60 g). A drink containing soluble beetroot crystals (BC; ∼1.40 mmol NO3-) and a control drink (CON; 70 mL deionised water) were also ingested. BP and plasma, salivary and urinary [NO3-] and [NO2-] were determined before and up to 24 h after ingestion. All NO3--rich vehicles elevated plasma, salivary and urinary nitric oxide metabolites compared with baseline and CON (P<0.05). The peak increases in plasma [NO2-] were greater in BF (371 ± 136 nM) and BR (369 ± 167 nM) compared to BL (283 ± 93 nM; all P<0.05) and BC (232 ± 51 nM). BR, but not BF, BL and BC, reduced systolic (∼5 mmHg) and mean arterial pressure (∼3-4 mmHg; P<0.05), whereas BF reduced diastolic BP (∼4 mmHg; P < 0.05). Although plasma [NO2-] was elevated in all conditions, the consumption of a small, concentrated NO3--rich fluid (BR) was the most effective means of reducing BP. These findings have implications for the use of dietary NO3-supplements when the main objective is to maintain or improve indices of cardiovascular health.

Acute acetaminophen ingestion improves performance and muscle activation during maximal intermittent knee extensor exercise.

AIM: Acetaminophen is a commonly used medicine for pain relief and emerging evidence suggests that it may improve endurance exercise performance. This study investigated some of the physiological mechanisms by which acute acetaminophen ingestion might blunt muscle fatigue development. METHODS: Thirteen active males completed 60 × 3 s maximum voluntary contractions (MVC) of the knee extensors with each contraction separated by a 2 s passive recovery period. This protocol was completed 60 min after ingesting 1 g of maltodextrin (placebo) or 1 g of acetaminophen on two separate visits. Peripheral nerve stimulation was administered every 6th contraction for assessment of neuromuscular fatigue development, with the critical torque (CT), which reflects the maximal sustainable rate of oxidative metabolism, taken as the mean torque over the last 12 contractions. Surface electromyography was recorded continuously as a measure of muscle activation. RESULTS: Mean torque (61 ± 11 vs. 58 ± 14% pre-exercise MVC) and CT (44 ± 13 vs. 40 ± 15% pre-exercise MVC) were greater in the acetaminophen trial compared to placebo (both P < 0.05). Voluntary activation and potentiated twitch declined at a similar rate in both conditions (P > 0.05). However, the decline in electromyography amplitude was attenuated in the acetaminophen trial, with electromyography amplitude being greater compared to placebo from 210 s onwards (P < 0.05). CONCLUSION: These findings indicate that acute acetaminophen ingestion might be ergogenic by increasing CT and preserving muscle activation during high-intensity exercise.

A randomised controlled trial exploring the effects of different beverages consumed alongside a nitrate-rich meal on systemic blood pressure.

BACKGROUND:: Ingestion of nitrate (NO3-)-containing vegetables, alcohol and polyphenols, separately, can reduce blood pressure (BP). However, the pharmacokinetic response to the combined ingestion of NO3- and polyphenol-rich or low polyphenol alcoholic beverages is unknown. AIM:: The aim of this study was to investigate how the consumption of low and high polyphenolic alcoholic beverages combined with a NO3--rich meal can influence NO3- metabolism and systemic BP. METHODS:: In a randomised, crossover trial, 12 normotensive males (age 25 ± 5 years) ingested an acute dose of NO3- (∼6.05 mmol) in the form of a green leafy salad, in combination with either a polyphenol-rich red wine (NIT-RW), a low polyphenol alcoholic beverage (vodka; NIT-A) or water (NIT-CON). Participants also consumed a low NO3- salad and water as a control (CON; ∼0.69 mmol NO3-). BP and plasma, salivary and urinary [NO3-] and nitrite ([NO2-]) were determined before and up to 5 h post ingestion. RESULTS:: Each NO3--rich condition elevated nitric oxide (NO) biomarkers when compared with CON ( P < 0.05). The peak rise in plasma [NO2-] occurred 1 h after NIT-RW (292 ± 210 nM) and 2 h after NIT-A (318 ± 186 nM) and NIT-CON (367 ± 179 nM). Systolic BP was reduced 2 h post consumption of NIT-RW (-4 mmHg), NIT-A (-3 mmHg) and NIT-CON (-2 mmHg) compared with CON ( P < 0.05). Diastolic BP and mean arterial pressure were also lower in NIT-RW and NIT-A compared with NIT-CON ( P < 0.05). CONCLUSIONS:: A NO3--rich meal, consumed with or without an alcoholic beverage, increases plasma [NO2-] and lowers systemic BP for 2-3 h post ingestion.

The mechanistic bases of the power-time relationship: muscle metabolic responses and relationships to muscle fibre type.

KEY POINTS: The power-asymptote (critical power; CP) of the hyperbolic power-time relationship for high-intensity exercise defines a threshold between steady-state and non-steady-state exercise intensities and the curvature constant (W') indicates a fixed capacity for work >CP that is related to a loss of muscular efficiency. The present study reports novel evidence on the muscle metabolic underpinnings of CP and W' during whole-body exercise and their relationships to muscle fibre type. We show that the W' is not correlated with muscle fibre type distribution and that it represents an elevated energy contribution from both oxidative and glycolytic/glycogenolytic metabolism. We show that there is a positive correlation between CP and highly oxidative type I muscle fibres and that muscle metabolic steady-state is attainable CP. Our findings indicate a mechanistic link between the bioenergetic characteristics of muscle fibre types and the power-time relationship for high-intensity exercise. ABSTRACT: We hypothesized that: (1) the critical power (CP) will represent a boundary separating steady-state from non-steady-state muscle metabolic responses during whole-body exercise and (2) that the CP and the curvature constant (W') of the power-time relationship for high-intensity exercise will be correlated with type I and type IIx muscle fibre distributions, respectively. Four men and four women performed a 3 min all-out cycling test for the estimation of CP and constant work rate (CWR) tests slightly >CP until exhaustion (Tlim ), slightly CP Tlim isotime to test the first hypothesis. Eleven men performed 3 min all-out tests and donated muscle biopsies to test the second hypothesis. Below CP, muscle [PCr] [42.6 ± 7.1 vs. 49.4 ± 6.9 mmol (kg d.w.)(-1) ], [La(-) ] [34.8 ± 12.6 vs. 35.5 ± 13.2 mmol (kg d.w.)(-1) ] and pH (7.11 ± 0.08 vs. 7.10 ± 0.11) remained stable between ∼12 and 24 min (P > 0.05 for all), whereas these variables changed with time >CP such that they were greater [[La(-) ] 95.6 ± 14.1 mmol (kg d.w.)(-1) ] and lower [[PCr] 24.2 ± 3.9 mmol (kg d.w.)(-1) ; pH 6.84 ± 0.06] (P < 0.05) at Tlim (740 ± 186 s) than during the

Dietary nitrate supplementation attenuates the reduction in exercise tolerance following blood donation.

We tested the hypothesis that dietary nitrate (NO3-)-rich beetroot juice (BR) supplementation could partially offset deteriorations in O2 transport and utilization and exercise tolerance after blood donation. Twenty-two healthy volunteers performed moderate-intensity and ramp incremental cycle exercise tests prior to and following withdrawal of ∼450 ml of whole blood. Before donation, all subjects consumed seven 70-ml shots of NO3--depleted BR [placebo (PL)] in the 48 h preceding the exercise tests. During the 48 h after blood donation, subjects consumed seven shots of BR (each containing 6.2 mmol of NO3-, n = 11) or PL (n = 11) before repeating the exercise tests. Hemoglobin concentration and hematocrit were reduced by ∼8-9% following blood donation (P < 0.05), with no difference between the BR and PL groups. Steady-state O2 uptake during moderate-intensity exercise was ∼4% lower after than before donation in the BR group (P < 0.05) but was unchanged in the PL group. The ramp test peak power decreased from predonation (341 ± 70 and 331 ± 68 W in PL and BR, respectively) to postdonation (324 ± 69 and 322 ± 66 W in PL and BR, respectively) in both groups (P < 0.05). However, the decrement in performance was significantly less in the BR than PL group (2.7% vs. 5.0%, P < 0.05). NO3- supplementation reduced the O2 cost of moderate-intensity exercise and attenuated the decline in ramp incremental exercise performance following blood donation. These results have implications for improving functional capacity following blood loss.

Two weeks of watermelon juice supplementation improves nitric oxide bioavailability but not endurance exercise performance in humans.

This study tested the hypothesis that watermelon juice supplementation would improve nitric oxide bioavailability and exercise performance. Eight healthy recreationally-active adult males reported to the laboratory on two occasions for initial testing without dietary supplementation (control condition). Thereafter, participants were randomly assigned, in a cross-over experimental design, to receive 16 days of supplementation with 300 mL·day(-1) of a watermelon juice concentrate, which provided ∼3.4 g l-citrulline·day(-1) and an apple juice concentrate as a placebo. Participants reported to the laboratory on days 14 and 16 of supplementation to assess the effects of the interventions on blood pressure, plasma [l-citrulline], plasma [l-arginine], plasma [nitrite], muscle oxygenation and time-to-exhaustion during severe-intensity exercise. Compared to control and placebo, plasma [l-citrulline] (29 ± 4, 22 ± 6 and 101 ± 23 µM), [l-arginine] (74 ± 9, 67 ± 13 and 116 ± 9 µM) and [nitrite] (102 ± 29, 106 ± 21 and 201 ± 106 nM) were higher after watermelon juice supplementation (P < 0.01). However, systolic blood pressure was higher in the watermelon juice (130 ± 11) and placebo (131 ± 9) conditions compared to the control condition (124 ± 8 mmHg; P < 0.05). The skeletal muscle oxygenation index during moderate-intensity exercise was greater in the watermelon juice condition than the placebo and control conditions (P < 0.05), but time-to-exhaustion during the severe-intensity exercise test (control: 478 ± 80, placebo: 539 ± 108, watermelon juice: 550 ± 143 s) was not significantly different between conditions (P < 0.05). In conclusion, while watermelon juice supplementation increased baseline plasma [nitrite] and improved muscle oxygenation during moderate-intensity exercise, it increased resting blood pressure and did not improve time-to-exhaustion during severe-intensity exercise. These findings do not support the use of watermelon juice supplementation as a nutritional intervention to lower blood pressure or improve endurance exercise performance in healthy adults.